ArticleProceedings of the National Academy of Sciences of the United States of America2007
TORC2 regulates germinal center repression of the TCL1 oncoprotein to promote B cell development and inhibit transformation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 27 citations in OpenAlex.
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- The regulatory interaction of EVI1 with the TCL1A oncogene impacts cell survival and clinical outcome in CLL.Leukemia · 2015Article
- AID-induced genotoxic stress promotes B cell differentiation in the germinal center via ATM and LKB1 signaling.Molecular cell · 2010Article
- Identification of a B cell signature associated with renal transplant tolerance in humans.The Journal of clinical investigation · 2010Article
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- TORC2, a coactivator of cAMP-response element-binding protein, promotes Epstein-Barr virus reactivation from latency through interaction with viral BZLF1 protein.The Journal of biological chemistry · 2009Article
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- Activation of TORC1 transcriptional coactivator through MEKK1-induced phosphorylation.Molecular biology of the cell · 2008Article
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- Interaction between TCL1 and Epac1 in the activation of Akt kinases in plasma membranes and nuclei of 8-CPT-2-O-Me-cAMP-stimulated macrophages.Cellular signalling · 2008Article
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Aberrant expression of the TCL1 oncoprotein promotes malignant transformation of germinal center (GC) B cells. Repression of TCL1 in GC B cells facilitates FAS-mediated apoptosis and prevents lymphoma formation. However, the mechanism for this repression is unknown. Here we show that the CREB coactivator TORC2 directly regulates TCL1 expression independent of CREB Ser-133 phosphorylation and CBP/p300 recruitment. GC signaling through CD40 or the BCR, which activates pCREB-dependent genes, caused TORC2 phosphorylation, cytosolic emigration, and TCL1 repression. Signaling via cAMP-inducible pathways inhibited TCL1 repression and reduced apoptosis, consistent with a prosurvival role for TCL1 before GC selection and supporting an initiating role for aberrant TCL1 expression during GC lymphomagenesis. Our data indicate that a novel CREB/TORC2 regulatory mode controls the normal program of GC gene activation and repression that promotes B cell development and circumvents oncogenic progression. Our results also reconcile a paradox in which signals that activate pCREB/CBP/p300 genes concurrently repress TCL1 to initiate its silencing.
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